The present issue of the Journal of Hypertension is focused on different dietary, clinical and therapeutic aspects of hypertension.
Mori et al. (pp. 421–428) have conducted a small but well designed randomized crossover study in controlled type 2 diabetes patients showing that drinking 230–300 ml/day of red wine slightly, although significantly, increases daytime SBP and DBP and slightly reduces asleep DBP without affecting glycaemic control or any other cardiovascular risk factor. In a population of nondiabetic adults without cardiovascular disease followed up for 5 years, baseline eating frequency was found by Karatzi et al. (pp. 429–437) to be associated with the rate of progression of pulse wave velocity, augmentation index, SBP and DBP and the incidence of new-onset hypertension, most of the associations remaining significant after adjustment for a number of variables including total energy intake.
Using administrative healthcare data in Stockholm County, Kristoferson Sandström et al. (pp. 414–420) have observed that both men and women with hypertension were more likely to have a diagnosis of depression and anxiety disorders, with slightly greater risk for men than women. In an accompanying editorial commentary, Smith and Graham (pp. 397–398) call attention on recent evidence of a possible biological link between bipolar disorder and hypertension, stimulated by the discovery from genome-wide association studies that calcium channels may play a role in both conditions. The authors suggest the possibility that treatments for hypertension, such as calcium-channel blockers, might in future be repurposed as treatments for mood disorders.
On the basis of a systematic review and meta-analysis of 13 studies on 2753 individuals, Cuspidi et al. (pp. 385–392) have calculated that the nondipping pattern of night-time blood pressure is associated with higher values of common carotid intima–media thickness and higher carotid plaque prevalence. In the Multi-Ethnic Study of Atherosclerosis, Atkinson et al. (pp. 410–413) have found that brachial artery diameter is significantly larger and its flow-mediated vasodilation is significantly smaller in patients with sleep apnoea, but the difference in flow-mediated vasodilation between patients with and without sleep apnoea loss significance when scaled for resting brachial artery diameter. Andreadis et al. (pp. 438–444) report that all the indices of preclinical organ damage in a group of untreated hypertensive patients strongly correlated with night-time blood pressure, either measured by ambulatory monitoring or by home automated measurement. In the prospective follow-up of nonhypertensive participants to the Korean Genome and Epidemiology Study, Kim et al. (pp. 524–531) have found that various indices of organ damage predict development of hypertension. In a cross-sectional study of hypertensive individuals, Mulé et al. (pp. 495–505) have observed that increasing severity of chronic kidney disease, assessed by estimated glomerular filtration rate, significantly correlates with aortic root diameter, suggesting that this may be one of the mechanisms whereby renal insufficiency is associated with increased cardiovascular risk. The relationship between renal and cardiovascular disease has also been approached in another study by Tanaka et al. (pp. 506–512). In 3599 nondiabetic and normotensive individuals, free of cardiovascular disease and with preserved glomerular filtration rate, followed-up for about 6 years, these authors report that another possible index of renal dysfunction, low-grade albuminuria, is a significant predictor of cardiovascular disease events and all-cause mortality. Population-attributable fractions for the top tertile of low-grade albuminuria related to cardiovascular disease events and all-cause mortality were 37.9 and 20.1%, respectively. In their editorial commentary to this article, Viazzi and Pontremoli (pp. 399–401) discuss pathogenetic mechanisms of microalbuminuria, and conclude that, despite uncertainties about these mechanisms, the finding of an increased urine albumin excretion provides the clinician with a clear message on cardiovascular health, and one that is worth using in clinical practice.
Three articles focus on relationship between hypertension and obesity. Barzel et al. (pp. 464–473) report that in rabbits, obesity-induced hypertension and increased renal sympathetic nerve activity appear to depend on the balance between greater activation of melanocortin signalling through melanocortin receptors and lesser activation of neuropeptide Y sympatho-inhibitory signalling. Ohlsson et al. (pp. 445–451), having genotyped 5453 individuals of the population-based Malmö Diet and Cancer Study, calculate that 1% of the Swedish population carries a phosphodiesterase 11A gene loss-of-function mutation associated with elevated blood pressure, abdominal obesity and risk of ischaemic stroke. Linhart et al. (pp. 402–409) have studied trends during 1980 to 2011 in hypertension prevalence in Fiji and found significant increase in both sexes and ethnicities, with significant contribution from obesity.
A large number of articles in this issue are devoted to therapeutic aspects of hypertension. Thomopoulos et al. (pp. 373–384) continue with their series of meta-analyses of blood pressure-lowering trials, this time focusing on new-onset heart failure as an outcome. They confirm that even when trials allowing enrolment of patients with baseline heart failure are excluded, heart failure remains with stroke, the cardiovascular outcome best prevented by antihypertensive treatment. They also suggest that the reduced ability of calcium antagonists in preventing heart failure when compared with that of other antihypertensive drug classes may be at least in part an effect of the experimental design used in comparative trials. The Systolic Hypertension Optimal Treatment (SHOT) trial investigators (pp. 393–396) illustrate the main reasons why their ongoing trial exploring different SBP targets in the treatment of elderly hypertensive patients with a previous stroke will continue after the recent publication of the results of the Systolic Blood Pressure Intervention Trial (SPRINT), the major reason being that SHOT is focused on a group of hypertensive patients (previous stroke) specifically excluded from SPRINT. Several practical aspects of antihypertensive treatment left open after SPRINT are also discussed.
Zdrojewski et al. (pp. 532–538) report their data on prevalence, awareness and control of hypertension in the elderly and very elderly in Poland, showing prevalence and awareness of hypertension decrease in nonagenarians whereas control among those treated increases. Fernald et al. (pp. 539–547) have analyzed data in the HEalthy Life in an Urban Setting (HELIUS) study and report that in the Netherlands, hypertension awareness and treatment rates are similar among different ethnic groups in both diabetic and nondiabetic patients, but adequate blood pressure control remains low among ethnic minorities. Sonawane et al. (pp. 548–557) report the results of a retrospective cohort study of the BlueCross-BlueShield of Texas database, showing that treatment modifications are common among newly treated hypertensive patients, and the rates significantly vary across antihypertensive drug classes. In an observational nationwide study in Taiwan, Shih et al. (pp. 567–575) have found that type 2 diabetic patients who initiated antihypertensive therapy based on either an angiotensin-converting enzyme inhibitor or an angiotensin receptor blocker had no significant difference in incident major cardiovascular events. This issue also reports the results of a recent, double-blind, randomized study comparing the blood pressure reducing efficacy of the angiotensin-converting enzyme inhibitor, zofenopril, and the angiotensin receptor blocker, irbesartan, both in combination with the diuretic, hydrochlorothiazide, in elderly individuals with isolated systolic hypertension showing that these patients respond well to both types of treatment (Modesti et al., pp. 576–587). Chang et al. (pp. 558–566) have used the Taiwan National Health Insurance claims database to further investigate the issue of the risk of breast cancer in women taking antihypertensive agents; their data suggest no association of the use of any antihypertensive medication and breast cancer risk, but call attention on the potential effect of confounding for indication.
Finally, a number of articles in this issue of the Journal of Hypertension are, as usual, focused on pathophysiological problems. Stead et al. (pp. 452–463) provide experimental evidence of development conditioning of endothelium-derived hyperpolarization factor-mediated vasodilatation in male mice of dams fed a fat-rich diet. Quadri and Siragy (pp. 486–494) conclude from their experiments that the (Pro)renin receptor contributes to the regulation of renal epithelial sodium channel through SGK-1-Nedd4-2 signalling pathway. Mølgaard et al. (pp. 513–523) show that hearts from spontaneous hypertensive stroke-prone rats with left ventricular hypertrophy are more vulnerable to ischaemia-reperfusion injury and identify mitochondrial complexes III and IV as possible foci of their increased vulnerability. In apolipoprotein E-null mice, Zhou et al. (pp. 474–485) report that a vaccine against the angiotensin II type-1 receptor, the ATRQβ-001 vaccine, reduce the progression of atherosclerosis. They also report that no obvious feedback of plasma renin–angiotensin system was elicited by the vaccine.
Conflicts of interest
There are no conflicts of interest.